Federica Piani1,2, Isabella Melena2, Cameron Severn2, Linh T Chung2, Carissa Vinovskis2, David Cherney3, Laura Pyle2,4, Carlos A Roncal-Jimenez1, Miguel A Lanaspa1, Arleta Rewers5, Daniël H van Raalte6, Wassim Obeid7, Chirag Parikh7, Robert G Nelson8, Meda E Pavkov9, Kristen J Nadeau2, Richard J Johnson1, Petter Bjornstad1,2. 1. Department of Medicine, Division of Renal Diseases and Hypertension, School of Medicine, University of Colorado, Aurora, Colorado, USA. 2. Department of Pediatrics, Section of Endocrinology, School of Medicine, University of Colorado, Aurora, Colorado, USA. 3. Department of Medicine, Division of Nephrology, School of Medicine, University of Toronto, Toronto, Ontario, Canada. 4. Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, Colorado, USA. 5. Department of Pediatrics, Section of Emergency Medicine, School of Medicine, University of Colorado, Aurora, Colorado, USA. 6. Diabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, VUmc, Amsterdam, The Netherlands. 7. Department of Medicine, Division of Nephrology, Johns Hopkins University, Baltimore, Maryland, USA. 8. Chronic Kidney Disease Section, Phoenix Epidemiology and Clinical Research Branch, NIDDK, Phoenix, Arizona, USA. 9. Division of Diabetes Translation, Center for Disease Control and Prevention, Atlanta, Georgia, USA.
Abstract
OBJECTIVE: Glomerular injury is a recognized complication of diabetic ketoacidosis (DKA), yet the tubular lesions are poorly understood. The aim of this prospective study was to evaluate the presence and reversibility of tubular injury during DKA in children with type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS: Blood and urine samples were collected from 40 children with DKA (52% boys, mean age 11 ± 4 years, venous pH 7.2 ± 0.1, glucose 451 ± 163 mg/dL) at three timepoints: 0-8 and 12-24 h after starting insulin, and 3 months after discharge. Mixed-effects models evaluated the changes in tubular injury markers over time (neutrophil gelatinase-associated lipocalin [NGAL], kidney injury molecule 1 [KIM-1], and interleukin 18 [IL-18]). We also evaluated the relationships among the tubular injury biomarkers, copeptin, a vasopressin surrogate, and serum uric acid (SUA). RESULTS: Serum NGAL, KIM-1, and IL-18 were highest at 0-8 h (306.5 ± 45.9 ng/mL, 128.9 ± 10.1 pg/mL, and 564.3 ± 39.2 pg/mL, respectively) and significantly decreased over 3 months (p = 0.03, p = 0.01, and p < 0.001, respectively). There were strong relationships among increases in copeptin and SUA and rises in tubular injury biomarkers. At 0-8 h, participants with acute kidney injury (AKI) [17%] showed significantly higher concentrations of tubular injury markers, copeptin, and SUA. CONCLUSIONS: DKA was characterized by tubular injury, and the degree of injury associated with elevated copeptin and SUA. Tubular injury biomarkers, copeptin and SUA may be able to predict AKI in DKA.
OBJECTIVE: Glomerular injury is a recognized complication of diabetic ketoacidosis (DKA), yet the tubular lesions are poorly understood. The aim of this prospective study was to evaluate the presence and reversibility of tubular injury during DKA in children with type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS: Blood and urine samples were collected from 40 children with DKA (52% boys, mean age 11 ± 4 years, venous pH 7.2 ± 0.1, glucose 451 ± 163 mg/dL) at three timepoints: 0-8 and 12-24 h after starting insulin, and 3 months after discharge. Mixed-effects models evaluated the changes in tubular injury markers over time (neutrophil gelatinase-associated lipocalin [NGAL], kidney injury molecule 1 [KIM-1], and interleukin 18 [IL-18]). We also evaluated the relationships among the tubular injury biomarkers, copeptin, a vasopressin surrogate, and serum uric acid (SUA). RESULTS: Serum NGAL, KIM-1, and IL-18 were highest at 0-8 h (306.5 ± 45.9 ng/mL, 128.9 ± 10.1 pg/mL, and 564.3 ± 39.2 pg/mL, respectively) and significantly decreased over 3 months (p = 0.03, p = 0.01, and p < 0.001, respectively). There were strong relationships among increases in copeptin and SUA and rises in tubular injury biomarkers. At 0-8 h, participants with acute kidney injury (AKI) [17%] showed significantly higher concentrations of tubular injury markers, copeptin, and SUA. CONCLUSIONS: DKA was characterized by tubular injury, and the degree of injury associated with elevated copeptin and SUA. Tubular injury biomarkers, copeptin and SUA may be able to predict AKI in DKA.
Authors: Isabella Melena; Federica Piani; Kalie L Tommerdahl; Cameron Severn; Linh T Chung; Alexis MacDonald; Carissa Vinovskis; David Cherney; Laura Pyle; Carlos A Roncal-Jimenez; Miguel A Lanaspa; Arleta Rewers; Daniël H van Raalte; Gabriel Cara-Fuentes; Chirag R Parikh; Robert G Nelson; Meda E Pavkov; Kristen J Nadeau; Richard J Johnson; Petter Bjornstad Journal: J Diabetes Complications Date: 2022-04-28 Impact factor: 3.219
Authors: Małgorzata Buksińska-Lisik; Przemysław Kwasiborski; Robert Ryczek; Wojciech Lisik; Artur Mamcarz Journal: J Clin Med Date: 2022-04-26 Impact factor: 4.964